Focused Transoesophageal Echo Assessment

Special thanks for the supervision and contribution to this page from:

Dr Jon Rosser

Consultant Cardiothoracic Anaesthetist and Intensivist. BSE TOE accredited.
Sheffield Teaching Hospitals

Dr Thanos Charalampopoulos - Consultant Cardiologist in Pulmonary Hypertension
Professor Robin Condliffe - Consultant Respiratory Physician
Sheffield Pulmonary Vascular Disease Unit

Written by Ben Stoney

1. Is the LV dilated?

The view to measure LV dilatation, within the fTOE dataset, is in the transgastric mid-papillary short axis view. The LV internal dimension in diastole (LVIDd) is taken.

End diastole can be determined in a few ways in this view, these are:

1. The frame where the LV is at its largest
2. The start of the QRS complex

Arrow demonstrating where to measure LVIDd.

Ensure that the LV is circular and not oval in shape, as this would suggest an oblique plane through the LV. This would lead to over-estimated LV cavity size. 

The measurement is taken using calipers to measure from the endocardial border of the mid-inferior wall to the mid-anterior wall of the LV.

It can be difficult to determine if the LVIDd measurement is taken perpendicular to the LV in this view. An alternative is to obtain the transgastric 2-chamber view. From the transgastric short axis view ensure the LV is in the centre of the image and then add 90 degrees of rotation sector angle. This will give an image of the LV in long axis and the LVIDd can be measured from there. 

BSE reference for LVIDd

LVIDd reference ranges are obtained from TTE images in the PLAX view at different LV walls and a slightly different LV level so may not correlate completely with TOE images. 

LV size

LVIDd Males

LVIDd Females


4.2-5.9 cm









>6.8 cm


Dilated LV cavity

  • Dilated cardiomyopathy
  • Ischaemic cardiomyopathy
  • Volume overload
  • Eccentric hypertrophy
  • Large person

Small LV cavity

  • Hypovolaemia 
  • Concentric hypertrophy
  • Small person

Small LV cavity with papillary muscle apposition in this case due to concentric hypertrophy from LVH.

2. Is the LV significantly impaired?

When assessing the function of the LV it is important to assess how the LV is contracting, but is also important to assess for any regional wall motion abnormalities (RWMAs), and any reduction in wall thickening and motion. This assessment is done by visual assessment of the LV. Basic global and regional LV assessment are covered below. 

Global LV systolic function

The LV can be assessed from the fTOE windows:

  • ME4Ch
  • ME2Ch
In fTOE the global systolic function is qualitatively assessed. This is a visual assessment which labels the LV as being ‘normal’ or ‘significantly impaired.’
Ejection fraction (EF) is a commonly used quantitative method to express LV function. This is calculated by the formula:
(SV =stroke volume and EDV = end diastolic volume)

Recent BSE guidance classifies LV ejection fraction as:
  • Normal LVEF ≥ 55%
  • Borderline LVEF 50-54%
  • Impaired LVEF 36-49%
  • Severely impaired LVEF ≤ 35%
So ‘normal’ LV function within fTOE could cover normal, borderline and impaired EF, essentially indicating that the LV function is not severely impaired. 

Global LV systolic function

TGSAX - significantly impaired LV function with anterolateral pericardial fluid.

ME4Ch - significantly impaired LV function


In health the LV contracts and the walls thicken and they move equally towards the centre of the LV cavity. Segmental assessment of the LV wall can help identify if there is a regional wall motion abnormality (RWMA) caused by reduced blood supply from a coronary artery. 

RWMAs can be due to ischaemia such as in an acute coronary syndrome. In this case, the RWMA will occur in the area supplied by the affected coronary artery territory. The myocardium in this area will display reduced excursion and wall thickening.


  • Normokinesia – normal endocardial motion and thickening
  • Hypokinesia – impaired endocardial motion and thickening
  • Akinesia – absent endocardial motion and thickening 
  • Dyskinesia – paradoxical outward movement of segment during systole

Blood supply to the heart

The main blood supply from the heart is from the left and right coronary arteries. The left coronary artery divides from the left main stem (LMS) into the left anterior descending artery and the left circumflex artery (LCx). 

RWMA assessment

The views in fTOE to assess for RWMAs are:

  • ME4Ch – anterolateral and inferoseptal wall
  • ME2Ch – anterior and inferior wall
  • MELAX – anteroseptal and inferolateral wall
  • TGMidSAX – all segments at mid-papillary level

ME4Ch - demonstrating anterolateral and inferoseptal wall

ME2Ch - demonstrating the anterior and inferior wall

MELAX - demonstrating the anteroseptal and inferolateral wall

↔︎ Slide across to show areas of blood supply. The TGSAX mid-papillary level is a good view to look for a RWMA as it shows segments supplied by all 3 major coronary arteries.

  • LAD – supplies the anterior and anteroseptal left ventricle
  • LCx – supplies the antero and inferolateral walls
  • RCA – supplies the inferoseptal and inferior walls

3. Is the RV dilated?

For more in depth look at transthoracic echocardiographic principles of right heart assessment than is covered here please visit the Right Heart Assessment page.

Within the fTOE dataset the main views from which right heart assessment takes place are:

  • ME4Ch 
  • ME RV inflow-outflow 
  • TG SAX

Assessment of RV size is generally best done in the ME4Ch view as the LV and RV can be seen together and the sizes compared. 

It is important that the RV is not foreshortened in this view and the widest diameter of the RV is seen. Forward rotation of the sector angle from 0-15 degrees may help with this. 

The RV size should be <2/3 of the size of the LV normally. If the RV > LV size then this indicates severe dilatation. 

Note which is the apex forming ventricle. Normally the LV is the apex forming ventricle. As the RV dilates it starts to form the apex with the LV and this would indicate at least moderate dilatation. 

RV severely dilatation - ME4Ch view showing RV > LV. The RV is forming the apex with the LV.

Interventricular septum

In both severe pressure and volume overload RV dilatation is seen with a flattened inter-ventricular septum on the TGSAX view (the LV becomes D-shaped). In normal circumstances the LV is circular with the inter-ventricular septum curved towards the RV. In conditions of pressure or volume overload the IVS can start to flatten and become D-shaped.

Depending on which phase of the cardiac cycle the IVS appears D-shaped will determine whether it is pressure or volume overload or a combination of the both.

  • Pressure overload – the IVS is D-shaped in systole
  • Volume overload – IVS is D-shaped in diastole, paradoxical septal motion may be present where hyperdynamic ventricles appear to move the septum anteriorly during systole.
  • Both pressure and volume overload – IVS appears D-shaped throughout both systole and diastole.

Volume overload - TGSAX - dilated RV with diastolic septal flattening.

Pressure and volume overload - TGSAX - systolic and diastolic septal flattening

4. Is the RV severely impaired?

One of the ways to assess RV function with TTE is with TAPSE, but this is more challenging with TOE. The main way of assessing RV function with fTOE is visual assessment and is categorised as ‘normal’ or ‘severely impaired.’

Due to the shape of the RV being triangular and wrapped around the LV, assessment should take place in as many views as possible.  

Fractional area change (FAC)

To help with visual assessment it is worth understanding fractional area change. 

In the ME4Ch view a trace of the endocardial border of the right ventricle is taken at end systole and end diastole. This obtains a measurement in cm².

FAC (%) = [(End diastolic area – end systolic area)/end diastolic area] x100











RV inflow-outflow view. Poor RV free wall contractility.
Note: Left coronary artery can be seen coming off next to the left coronary cusp of the AV.

Posterior mitral valve prolapse leading to echo features of right heart strain (dilated and impaired RV). Combined with systolic and diastolic septal flattening - indicating pressure and volume overload. Mild TR. Pulmonary artery catheter in-situ confirmed raised pulmonary artery pressures.

5. Is there significant valvular pathology?

The key components to the assessment of valves are:

  • Visual assessment
  • Colour flow Doppler


Perform 2D visual assessment of aortic, mitral and tricuspid valves from all available views, assessing for:

  • Thickness, calcification, mobility
  • Forward/backward flow through the valve
  • Any flail or prolapse?
  • Any masses adherent to the valve?
  • Any destruction of the valve?


Assess valves with colour flow doppler, looking for regurgitation and flow acceleration. 

Ensure that the echo beam plane is fanned through the whole of the valve in each view. This will help determine where the regurgitation is maximal. 


  • Box size – should cover the whole of the valve and the chamber which the regurgitant jet flows into 
  • Nyquist limit – assessing regurgitation should be set to 50-70cm/s
  • Vena contracta – size is proportional to size of regurgitant orifice
  • Flow convergence and jet area – both represent regurgitant volume


  • Eccentric regurgitant jets into chamber walls will have reduced velocity and look less severe.
  • Haemodynamic instability will affect the pressure gradient across valves – e.g. low systolic BP will lead to reduced velocity of mitral regurgitation (if present) leading to underestimation.  

Aortic valve assessment


Aortic valve assessment can take place in both long axis and short axis. The best views from the fTOE dataset are:

  • MELAX – reduce depth to focus on AV
  • AV SAX – with slight angle modification to the RV inflow/outflow view

Anatomy of aortic valve

The aortic valve is tricuspid with the three leaflets named after the coronary artery which arises from the associated sinus. 
These are called the right, left and non-coronary cusps (indicated with R, L, N in the images across). 

ME AV SAX - Tricuspid aortic valve with LCA visualised. RCC sits over the RVOT, NCC is always on the intra-atrial septum.

ME AV LAX - Right coronary cusp is always the lowermost leaflet, (next to the RVOT). Also demonstrated in the SAX view above.

Aortic Stenosis

Abnormalities of aortic valve

The commonest causes of aortic valve degeneration leading to stenosis are:
  • Calcific
  • Bicuspid aortic valve
  • Rheumatic 

Visualisation of the valves thickness, mobility and calcification is important. 

Clinical features of severe aortic stenosis

  • Syncope
  • Angina
  • Dyspnoea

Echo assessment aortic stenosis

  • Visual
    • Thickened/calcified aortic valve leaflets
    • Reduced mobility of valve
    • Reduced leaflet opening
  • Colour flow doppler
    • Increased flow velocity/turbulent flow
    • At the valve level and into the aorta

Other echo features in severe AS

  • Look for aortic regurgitation and other valvular abnormalities
  • Look for evidence of left ventricular hypertrophy
  • Look for aortic root dilatation 

ME AV SAX - tricuspid AV, with calcification (bright white) and thickened leaflets, restricted opening. Visually severe AS.

ME AV LAX - thickened, calcified, restricted opening. Severe AS.

Turbulent flow on colour doppler at valve level and into aorta.

Aortic Regurgitation

Echo assessment aortic regurgitation

  • Visual
    • Valve prolapse?
    • Vegetations consistent with infective endocarditis?
    • Aortic root dilatation or dissection flap?
  • Colour flow doppler
    • Jet extension back into LV – not a reliable marker of severity
    • Width of Jet in LVOT (within 1cm of AV)
    • Vena contracta width (narrowest region of colour flow at AV level) 

Other echo features in aortic regurgitation

  • Look for aortic stenosis and other valvular abnormalities
  • Look for evidence of left ventricular dilatation
  • Look for aortic root dilatation 
Severity of aortic regurgitation
  • VC width >0.6cm is severe
    • This cannot be measured if more than one regurgitant jet
  • Jet width ratio with LVOT >65% is severe
    • This is misleading in eccentric jets

For the fTOE curriculum measurements of the vena contracta or jet width ratio with the LVOT are not expected, but these values help to give an idea of what severe aortic regurgitation may look like visually. 


ME AV LAX - right coronary cusp prolapse. Large space between valve leaflets at end-systole.

ME AV LAX - large eccentric regurgitant jet indicating severe AR.

Mitral valve assessment


Mitral valve assessment should take place in all views in which the mitral valve is seen. The best views from the fTOE dataset are:

  • MEA4Ch
  • MEA2Ch

Anatomy of mitral valve

The mitral valve is made up from the mitral valve annulus, two mitral valve leaflets (anterior (AML) and posterior (PML)) and the subvalvular apparatus (the papillary muscles and chordae tendineae).

There are two papillary muscles:
  • Posteromedial papillary muscle – attached to mid-inferior LV wall
  • Anterolateral papillary muscle – attached to mid-anterolateral LV wall

The papillary muscles attach to the mitral valve via the chordae tendinae, and each papillary muscle supplies chordae that attach to both mitral valve leaflets.   

Transgastric short-axis mid-papillary level

↔︎ Slide across to visualise the blood supply of the papillary muscles on this image

The posteromedial papillary muscle has a sole blood supply by the RCA meaning it is the papillary muscle that most commonly ruptures with ischaemia. 

The anterolateral papillary muscle has a dual blood supply from the LAD and LCx.

Mid-oesophageal 4-chamber

Note the location of mitral valve leaflets

Mid-oesophageal 2-chamber

Note the location of mitral valve leaflets

Mid-oesophageal long-axis

Note the location of mitral valve leaflets

Mitral Stenosis

Abnormalities of mitral valve

The commonest causes of mitral valve degeneration are:
  • Mitral annular calcification 
  • Rheumatic 

Visualisation of the valves thickness, mobility and calcification is important. 

Echo assessment mitral stenosis

  • Visual
    • Thickened/calcified mitral valve leaflets
    • Reduced mobility of valve
    • Reduced leaflet opening
    • ‘Hockey stick’ sign 
  • Colour flow doppler
    • Increased flow velocity/turbulent flow
    • At the valve level of the mitral valve and into the left ventricle 

Other echo features in severe mitral stenosis

  • Dilated LA +/- spontaneous echo contrast
  • AF
  • Pulmonary hypertension
  • RV dilatation or dysfunction 
  • Tricuspid regurgitation

Restricted posterior mitral valve leaflet mobility, with thickening and calcification. Spontaneous echo contrast in a dilated left atrium.

Restricted mitral valve opening, with turbulent colour flow across the valve, some mild mitral regurgitation. Note anterior mitral valve 'hockey stick' sign

Severely restricted mitral valve opening with thickening and calcification. Increased colour flow doppler at mitral valve level into the left ventricle. Some mild-moderate mitral regurgitation.

Dilated LA with spontaneous echo contrast in severe MS. See assessment of left atrial appendage below

These patients are high risk for left atrial thrombus (seen above).

Mitral Regurgitation

Echo assessment mitral regurgitation

  • Visual
    • Valve prolapse or flail?
    • Vegetations consistent with infective endocarditis?
    • Calcification/thickening?
    • Annular dilatation?
  • Colour flow doppler
    • Jet extension back into LA 
    • Vena contracta width (narrowest region of colour flow at MV level) 
    • Size of PISA/flow convergence 

Flail vs. prolapse

  • Prolapse = body and tip of the leaflet lie above the annular plane at end systole and leaflet tip points towards the LV

  • Flail = body and tip of the leaflet lie above the annular plane at end systole and leaflet tip points towards the LA

Posterior mitral valve prolapse with a dilated and impaired RV. Note the echobright line in the RV is a pulmonary artery catheter and signs of right heart strain.

Anterior mitral valve leaflet flail due to papillary muscle rupture. Note hyperdynamic LV.

Eccentric regurgitant jet into the LA and very large vena contracta - indicating severe mitral regurgitation

References for severe mitral regurgitation



Flail or prolapse


Very large regurgitant jet area
Ratio of jet area to LA area >40%
VC width ≥0.7cm
PISA radius >1cm

Causes of mitral regurgitation

(leaflet abnormality)

(ventricule remodelling)

Prolapse, flail, rupture


Degeneration, calcification

Non-ischaemic cardiomyopathy

Infective endocarditis, vegetations

Annular dilatation

Inflammatory - rheumatic


Causes of mitral regurgitation

Acute mitral regurgitation
Echo features

  • LV & LA are normal size
  • LV appears hyperdynamic

Clinical features

  • Sudden onset
  • Severe breathlessness
  • Hypotension and cardiogenic shock
  • Acute coronary syndrome
  • Acute pulmonary oedema
Chronic mitral regurgitation
Echo features
  • Enlarged LA, LV and RV
  • Normal/reduced LV contractility

Clinical features

  • Gradual onset 
  • Slowly progressive breathlessness on exertion
  • Atrial fibrillation
 Indirect indicators of severity of MR
  • LA dilatation
  • LV dilatation
  • LV dysfunction
  • Pulmonary hypertension

Systolic anterior motion of the mitral valve

Systolic anterior motion (SAM) of the anterior mitral valve leaflet is a dynamic LVOT obstruction. It usually occurs with hypertrophic cardiomyopathy, it may occur after mitral valve repair or aortic valve replacement. 

There is a reduced distance between the anterior mitral valve leaflet and ventricular septum in systole – usually due to LV septal hypertrophy. There is flow acceleration through the narrowing causing a drag effect pulling the anterior mitral valve leaflet into the LVOT. 

This leads to both turbulent flow in the LVOT and mitral regurgitation on colour doppler. 

Systolic anterior motion of the anterior mitral valve leaflet into the LVOT

SAM. Note the turbulent flow in the LVOT and the mitral regurgitation into the LA.

SAM. Note the turbulent flow in the LVOT and the mitral regurgitation into the LA.

Tricuspid valve assessment


The best views for tricuspid valve assessment are:

  • RV inflow view (RVI)
  • PSAX – aortic valve level
  • A4Ch

Anatomy of tricuspid valve

The tricuspid valve as the name suggests is made up from 3 leaflets. The septal, anterior and posterior leaflets. 

Causes of tricuspid valve disease
Tricuspid valve regurgitation is commonly caused by:
  • Rheumatic disease
  • Infective endocarditis
  • Carcinoid
  • Valve prolapse
  • Annular dilatation – secondary to RV dilatation (functional TR) 
  • Pacing wire passing into RV
Tricuspid stenosis is commonly caused by rheumatic fever and will have accompanying mitral stenosis. Rarer causes of tricuspid stenosis is carcinoid which commonly also affects the pulmonary valve (right heart valves). 

Mid-oesophageal 4-chamber

RV inflow-outflow

Tricuspid Regurgitation

A small amount of tricuspid regurgitation is present in about 70% of individuals with a structurally normal heart. 

Echo features of tricuspid regurgitation

  • Visual inspection
    • Look at annulus, leaflets, papillary muscles and chordae
    • Look at thickness, mobility, calcification and for signs of prolapse
  • Colour
    • Jet area >10cm²
    • VC width ≥0.7cm

Severe TR and RV dilatation

This is the same clip as the one above without the colour doppler. Note the lack of movement of the anterior leaflet of the tricuspid valve. This was caused by restriction from a pacing wire.

Infective endocarditis

TOE is a better modality for visualising endocarditis than TTE. It is seen as a vegetation one or more of the cardiac valves. It is more commonly seen on the aortic or mitral valve than the tricuspid or pulmonary valve. Right sided endocarditis is more likely in intravenous drug use. 

Echocardiographic features of endocarditis:

  • Irregularly shaped vegetation
  • Echogenic
  • Independent oscillatory motion
  • Moves with cardiac cycle
  • Low pressure side of the heart valve

Endocarditis may cause valve stenosis or new regurgitation. 

Thrombi and vegetations display similar echocardiographic properties. Vegetations from infected material lead to regurgitant lesions, valvular perforation, abscess formation which can all help distinguish it from thrombus formation. 


Aortic valve endocarditis - irregularly shaped vegetation, echogenic, low pressure side of valve.

Non-coronary cusp aortic valve endocarditis

MVR thrombus - the appearance of which is similar to endocarditis.

6. Is there pericardial or pleural fluid?

Pericardial fluid

Pericardial fluid can accumulate as a result of effusions (e.g. infective, malignant, uraemic) or bleeding (e.g. aortic dissection, post-op cardiac surgery). 

The echocardiographic features of pericardial fluid are that is is generally anechoic (black) and for it to be pericardial the fluid needs to be between the myocardium and the pericardium. It is normal to see very small amounts of pericardial fluid in some patients. The pericardial collection can either be concentric or localised. 

The pericardial effusion size can be measured at end diastole perpendicular to the pericardium and myocardium. { fluid can accumulate as a result of effusions (e.g. infective, malignant) or bleeding (e.g. aortic dissection, post-op cardiac surgery). Maximal measurements around each regional wall should be made.

Pericardial effusion size
Small < 0.5cm 
Moderate 0.5-2cm
Large >2cm

The appearance of the effusion can help distinguish its cause:

  • Simple effusion – uniform, anechoic
  • Exudative/fibrinous – stranding/loculation
  • Old blood – echogenic & grainy
  • Acute blood – similar to simple serous effusion
  • Purulent effusion – echogenic

TGSAX view - Loculated pericardial effusion

TGSAX view - large pericardial collection with clot formation. This is causing signfiiciant LV and RV collapse.

ME4Ch - large pericardial collection causing compression and some collapse of the RA.

Cardiac tamponade

Echocardiographic features of cardiac tamponade


  • IVC dilated, not collapsing
  • RA collapse 

Late sign:

  • RV early diastolic collapse → significant haemodynamic compromise

Very late sign:

  • LV/LA collapse
It is important to use the clinical picture to help determine whether a patient has cardiac tamponade. 

RV inflow-outflow view with large pericardial collection causing RV compression

Pleural fluid

Pleural fluid can be assessed from the mid-oesophageal view with the sector angle at 0 degrees. By rotating the probe to the patients left (anti-clockwise), the left pleural space can be assessed. By rotating the probe to the patients right (clockwise), the right pleural space can be assessed. 

Left pleural space

This can be identified as the left as the descending thoracic aorta can be seen at the top of the image. 

Left pleural space - descending thoracic aorta at the top of the image. Pleural fluid can be seen as anaechoic and crescent shaped below. To the bottom left of the image is collapsed/consolidated lung tissue.

Right pleural space - large pleural fluid collection seen as anechoic cresent shaped. The lung is to the right of the image on this side. Again this can be seen as collapsed and poorly aerated.

7. Is there aortic pathology

The ascending aorta, the arch of the aorta and descending aorta can all be visualised using TOE. With the fTOE windows the ascending aorta can be assessed in long axis and the descending aorta in short axis. The main pathologies that may be visualised are:

  • Dilated ascending aorta
  • Aortic dissection flap
  • Atheroma
  • Location of IABP tip

Aortic Root and proximal ascending aorta ⁶

Proximal ascending aorta can be measured in the ME Ascending Aorta Long Axis view. 

The aortic root is comprised of the aortic annulus, the sinus of valsalva and the sinotubular junction. As the aortic root and proximal ascending aorta dilates there is loss of the sinotubular junction curvature. Dilatation of the aortic root can lead to aortic insufficiency.

Measurement of proximal ascending aorta:

  • Inner edge to inner edge
  • End diastole 
  • 3cm above the aortic valve – in line with the right pulmonary artery. 

A value >40mm indicates dilated proximal ascending aorta. 


Dilated ascending aorta 4.94cm measured at the level of the right pulmonary artery in short axis (seen just above the aorta).

Dilated proximal ascending aorta with loss of sinotublar junction.

Aortic dissection

Aortic dissection is caused by an intimal tear (inner layer) in the aortic wall and allows blood to enter into the middle layer (media). This blood travels proximally and distally from the tear and causes the inner and outer wall of the aorta to dissect. 

The commonly used classification is Stanford classification and is classified as:

  • Stanford A – all dissections involving the ascending aorta – these are treated as a surgical emergency.
  • Stanford B – all dissections not involving the ascending aorta – these are managed medically unless complications arise.
Type A aortic dissections have twice the mortality of the type B dissections (25% vs 12%). The commonest cause of death is aortic rupture followed by aortic regurgitation which leads to heart failure and cardiogenic shock.⁵ 

Type A aortic dissection with intimal flap prolapse through the aortic valve


Common complications of aortic dissection⁵

  • Aortic regurgitation (40-75% of type A)
  • Cardiac tamponade (<20% of type A)
  • Cardiac ischaemia (10-15%)
  • Cardiogenic shock (<10%)
  • Stroke (<10%)
  • Large pleural effusion (15-20%)
  • Lower limb ischaemia (<10%)
  • Organ malperfusion 
    • Spinal cord ischaemia (1%)
    • Mesenteric ischaemia (<5%)
    • Acute renal failure (<20%)
Causes of aortic regurgitation in aortic dissection 
  • Aortic root dilatation – leading to coaptation defect 
  • Cusp prolapse – if the dissection extends and disrupts the attachment of the aortic valve leaflet/s.
  • Dissection flap prolapse – in diastole the the intimal flap prolapses through the aortic valve causing aortic regurgitation.

Intimal flap at the level of the aortic valve

Severe aortic regurgitation caused by intimal flap prolapse

Cardiac ischaemia

This is caused by extension of the false lumen of the dissection causing compression of the coronary ostia. It can also be caused by extension of the dissection down a coronary artery. This will lead to cardiac ischaemia with ST changes on ECG and regional wall motion abnormalities on echocardiography. 

RWMA seen in the anterior wall of the LV (right of the clip) in a patient with type A aortic dissection. There is reduced endocardial excursion and thickening indicating hypokinesia. Compare to the inferior wall (left of image). The false lumen is likely compressing the left coronary artery ostia.

True vs false lumen ⁶

The simplest way to identify the false lumen is most of the time the false lumen is larger than the true lumen. 

True lumen

False lumen



Normal colour flow

Reduced flow on colour doppler

Spontaneous echo contrast

Expands in systole

Intimal flap towards true lumen in diastole

True vs false lumen - true lumen smaller, expands systole, smaller in diastole. False lumen - spontaneous echo contrast.

Normal colour flow on doppler in true lumen (which is smaller than false lumen) and no flow on colout doppler in false lumen.


Aortic atheroma may be visualised on fTOE whilst imaging the aorta. Aortic atheromas are associated with coronary artery disease, peripheral vascular disease, aortic stenosis and mitral annular calcification. They pose a potential source of embolisation and increase the risk of cerebrovascular disease. ¹ ⁶ 

TOE appearance

Atheroma appearance on TOE:

  • Irregular intimal thickening ≥ 2mm
  • Increased echogenicity
  • Potential mobile or ulcerated components
The Katz classification grades atheroma severity. 
  • Severe atheroma >5mm
  • Complex atheroma = Mobile or ulcerated components

Severe atheroma - Irregular intimal thickening >5mm, increased echogenicity

Severe atheroma - with potential mobile component

8. Left atrial appendage thrombus

The left atrial appendage is a common area for thrombus formation due to its potential for lower blood velocity and stasis. The risk of LAA thrombus is increased if the patient is in AF where there is no coordinated atrial contraction or if there is low left atrial blood velocity in conditions such as mitral stenosis or cardiomyopathy with left atrial dilatation. The presence of spontaneous echo contrast indicates that blood velocity is low and is also a high risk feature for LAA thrombus.

Left atrial appendage thrombus on fTOE

The LAA can be visualised from a modified ME2Ch view in fTOE by bringing the LAA into the centre of the image. 

Attempt to visualise thrombus formation within the LAA and scan through the whole of the LAA to do this. X-plane if available can be useful to visualise two planes of the LAA at once. Fresh thrombus may be difficult to visualise (similar to DVT scanning). 

Look for risk factors for LAA thrombi like AF, spontaneous echo contrast or low exiting velocity using PW-doppler. 

Exiting velocities are assessed using PW-doppler placed within 1cm of the LAA ostium. If the peak velocity is ≤20cm/s there is an increased risk of LAA thrombus. 

Spontaneous echo contrast (SEC) or 'smoke' in the LAA

Subtle LAA thormbus

Large LAA thrombus extending into the LA

A patient with mitral stenosis, spontaneous echo contrast and LAA thrombus.

9. Patent foramen ovale

The term patent foramen ovale is given to communication between the left and right atrium where there is no defect in the septal tissue as would be the case for an atrial septal defect. 

The foramen ovale closes naturally in most people within a few months after birth, but can remain patent in up to 25-30% of the population. 

A PFO generally occurs between the membranous and muscular part of the atrial septum (at the superior border of the fossa ovalis). 

In normal haemodynamic conditions the LA pressure is higher than the RA pressure and so there is little to no flow from the right to the left. In conditions leading to a raised right atrial pressure (such as pulmonary hypertension or RV dysfunction) this can cause blood to flow from the right atrium to the left atrium causing a right-to-left shunt. This can lead to issues with hypoxaemia but also with paradoxical embolisation leading to stroke. 


The PFO can be visualised on the ME bicaval view. Placing colour flow doppler over the fossa ovalis and looking for a communicating jet across the atrial septum. The nyquist limit may need to be reduced to help visualise the PFO.

Fossa ovalis between the LA (above) and the RA (below).

Colour flow doppler demonstrating the PFO demonstrating right to left flow.

'Bubble' echo

Injected agitated saline can be used to help diagnose a PFO or right-to-left shunt and is used across the TTE, TOE and TCD modalities. 

  • TOE – ME bicaval or ME4Ch view
  • TTE – A4Ch view
  • TCD 

10ml of 0.9% saline is rapidly drawn between two syringes using a three-way tap (no air needed), to agitate the saline. The three-way tap is attached to a central or peripheral line and then rapidly injected after agitation has occurred. 

The ‘microbubbles’ from the saline will opacify the right heart. For a positive test either ‘microbubbles’ are seen crossing the atrial septum or there are bubbles within the left atrium within 3-5 cardiac cycles. If the shunt is intra-cardiac this is usually within 4 seconds of RA contrast opacification, if there is an intra-pulmonary shunt there will be a delay in ‘microbubbles’ entering the LA, which is usually more than 4 seconds.  


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  2. Complications related to peri-operative transoesophageal echocardiography – a one-year prospective national audit by the Association of Cardiothoracic Anaesthetists and Critical Care. Ramalingham, G. et al. Anaesthesia 2020, 75, 21-26
  3. Critical care transesophageal echocardiography. Mayo, P. et al. Chest. July 2015. 148(5); 1323-1332
  4. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases. European heart journal, 2014. 35,2873–2926. doi:10.1093/eurheartj/ehu281
  5. Echocardiography in aortic disease: EAE recommendations for clinical practice. Evangelista, A. et al. European journal of echocardiography. (2010)11,645–658 

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